Open AccessCD4‐independent binding of HIV‐1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody
Author(s) -
MONTEFIORI D. C.,
ZHOU J.,
SHAFF D. I.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb05855.x
Subject(s) - antibody , biology , complement system , complement receptor , immunology , virology , receptor , complement receptor 1 , antibody dependent enhancement , alternative complement pathway , virus , viral replication , biochemistry
SUMMARY Complement and antibody contribute to infection‐enhancement and possible expanded cellular tropism of HIV‐1 in vitro through a process requiring complement receptors. Until now, however, the ability of HIV‐1 to bind complement receptors has not been documented or characterized. We investigated whether antibody and complement permitted HIV‐1 to bind to the B lymphocyte receptor, CR2 (CD21), in an effort to learn more about infection‐enhancement, and also because CR2 can mediate B cell proliferation and antigen localization in lymphoid organs in other systems. HIV‐1 incubated with antibody and fresh human serum as a source of complement bound approximately 10‐fold greater to cells expressing CR2 than to HIV‐1‐permissive cells lacking this receptor. A similar effect was observed using cells which expressed CR2 but no CD4. This binding was minimal in heat‐inactivated and C3‐deficient sera, and was significantly reduced by the anti‐CR2 MoAb, OKB7, but not by the anti‐CD4 MoAb, OKT4a. Thus, complement and antibody acted in concert to facilitate the binding of HIV‐1 to CR2 independently of CD4. CD4‐independent binding of HIV‐1 to CR2 was not sufficient to produce infection in Raji‐3 cells. Titres of antibodies mediating CR2 binding correlated with antibody titres as measured by immunofluorescenee ( P < 0.01) and infection‐enhancement ( P < 0.05) but were discordant with titres of neutralizing antibodies, a result consistent with the utilization of CR2 for enhanced infection of cells. The ability of complement and antibody to facilitate the binding of HIV‐1 to CR2 in the absence of CD4 provides new insights into mechanisms of HIV‐1‐induced immunopathogenesis and infection‐enhancement.